Endothelial dysfunction: cardiovascular risk factors, therapy, and outcome.

TLDR

Endothelial dysfunction, a well‑established response to cardiovascular risk factors, precedes atherosclerosis and promotes lesion formation via adhesion molecule up‑regulation, chemokine secretion, leukocyte adherence, increased permeability, LDL oxidation, platelet activation, cytokine release, and vascular smooth muscle proliferation, and it is reversible with risk‑factor treatment and predicts cardiac events. The review aims to examine endothelial dysfunction’s pathogenesis, treatment options, and clinical outcomes. The authors conduct a literature review of studies on endothelial dysfunction’s mechanisms, therapeutic interventions, and prognostic implications.

Abstract

Endothelial dysfunction is a well established response to cardiovascular risk factors and precedes the development of atherosclerosis. Endothelial dysfunction is involved in lesion formation by the promotion of both the early and late mechanisms of atherosclerosis including up-regulation of adhesion molecules, increased chemokine secretion and leukocyte adherence, increased cell permeability, enhanced low-density lipoprotein oxidation, platelet activation, cytokine elaboration, and vascular smooth muscle cell proliferation and migration. Endothelial dysfunction is a term that covers diminished production/availability of nitric oxide and/or an imbalance in the relative contribution of endothelium-derived relaxing and contracting factors. Also, when cardiovascular risk factors are treated the endothelial dysfunction is reversed and it is an independent predictor of cardiac events. We review the literature concerning endothelial dysfunction in regard to its pathogenesis, treatment, and outcome.